Long Non-coding RNA TUG1 Promotes Parkinson's Disease via Modulating MiR-152-3p/PTEN Pathway

Kaihua Zhai, Boyu Liu, Lin Gao
Human Gene Therapy 2020 August 18
Long non-coding RNA taurine up-regulated gene 1 (TUG1) participates in nervous system diseases, but its function in Parkinson's disease remains unclear. This study explored the function and mechanism of TUG1 in Parkinson's disease (PD). A PD model was constructed using SH-SY5Y cells induced by 1-methyl-4-phenylpyridinium (MPP+) in vitro and mice treated by 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in vivo. The expressions of TUG1, miR-152-3p, phosphatase and tensin homolog (PTEN), tyrosine hydroxylase (TH), Bcl-2, cleaved caspase-3 expressions were determined by quantitative reverse transcription-PCR (qRT-PCR) and Western blotting. The viability, apoptosis, reactive oxygen species and release of inflammatory factors from SH-SY5Y cells and substantia nigra tissues were detected by commercial kits. The interaction between TUG1 and miR-152-3p were analyzed by dual-luciferase reporter assay. Hematoxylin-eosin (HE) and Immunohistochemical (IHC) staining were performed for assessing the pathological damage and proportion of TH-positive cells. In PD cell model and mice model, TUG1 expression was up-regulated and that of miR-152-3p was down-regulated. Further research showed that TUG1 sponged and regulated miR-152-3p expression. Silencing of TUG1 not only protected SH-SY5Y cells against cell apoptosis, oxidative stress and neuroinflammation in vitro, pathological damage and neuroinflammation in vivo, but also suppressed the expressions of PTEN and cleaved caspase-3, increased the expressions of TH and Bcl-2 in MPP+-treated SH-SY5Y cells. However, the protective role of siTUG1 in SH-SY5Y cells was significantly inhibited by miR-152-3p inhibitor. Thus, knocking down TUG1 might have a protective effect on PD through miR-152-3p/PTEN pathway.

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